The ubiquitin- and SUMO-dependent signaling response to DNA double-strand breaks

被引:92
作者
Bekker-Jensen, Simon [1 ]
Mailand, Niels [1 ]
机构
[1] Univ Copenhagen, Ubiquitin Signaling Grp, Dept Dis Biol, Novo Nordisk Fdn Ctr Prot Res, DK-2200 Copenhagen, Denmark
关键词
DNA double-strand break; Ubiquitin; SUMO; Chromatin; DNA repair; DAMAGE RESPONSE; HISTONE UBIQUITINATION; STRUCTURAL BASIS; REPAIR; BRCA1; PHOSPHORYLATION; UBIQUITYLATION; METHYLATION; DOMAIN; 53BP1;
D O I
10.1016/j.febslet.2011.05.056
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
DNA double-strand breaks (DSBs) represent the most destructive type of chromosomal lesion and trigger rapid chromatin restructuring accompanied by accumulation of proteins in the vicinity of the DSB. Non-proteolytic ubiquitylation of chromatin surrounding DSBs, mediated by the RNF8/RNF168 ubiquitin ligase cascade, has emerged as a key mechanism for restoration of genome integrity by licensing the DSB-modified chromatin to concentrate genome caretaker proteins such as 53BP1 and BRCA1 near the lesions. In parallel, SUMOylation of upstream DSB regulators is also required for execution of this ubiquitin-dependent chromatin response, but its molecular basis is currently unclear. Here, we discuss recent insights into how ubiquitin-and SUMO-dependent signaling processes cooperate to orchestrate protein interactions with sites of DNA damage to facilitate DSB repair. (C) 2011 Federation of European Biochemical Societies. Published by Elsevier B.V. All rights reserved.
引用
收藏
页码:2914 / 2919
页数:6
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